Three million years ago, a gene mutation switched off a sugar-making enzyme in early hominids. Our ancestors actually became unable to breed with those who still had the enzyme, possibly causing the emergence of our evolutionary grandparent, Homo erectus.

All animal cells are covered in a specific type of sugar molecule known as sialic acids. These molecules are an essential part of every cell's interaction with other cells and the wider environment, which means they're often the first point of contact between the cell and dangerous pathogens. All living apes except humans share a particular type of siliac acid, called N-glycolylneuraminic acid, or Neu5Gc.


Until about three million years ago, our hominid ancestors also carried Neu5Gc, along with all the other apes. But then a gene mutation caused the enzyme responsible for making Neu5Gc to switch off. We don't know why this mutation took hold, although one possibility is that a particularly virulent strain of malaria wreaked havoc on Neu5Gc, which meant hominids that could do without that particular sugar molecule would have an adaptive advantage.

To compensate for the loss of Neu5Gc, some hominids started producing more of a related siliac acid, Neu5Ac. What's more, they actually started to develop a resistance in their immune systems to Neu5Gc. UC San Diego evolutionary biologist Pascal Gagneux explains:

"This occurred at about the same time as early humans were apparently becoming major predators in their environment. It's hard to be sure exactly what happened because evolution works on so many things simultaneously, but the change in sialic acid meant that early humans developed an immune response to Neu5Gc. It became viewed by their immune systems as foreign, something to be destroyed. At about the same time, they started eating red meat, a major source of Neu5Gc, which may have further stimulated the immune response."


The key here is that some hominids still carried Neu5Gc while others had now developed an immune response against this sugar molecule. Now, imagine what would happen if a male from the first group tried to mate with a female from the second group. The male's Neu5Gc-carrying sperm would be targeted and destroyed by the female's Neu5Gc-resistant immune system.

It would suddenly become extremely difficult for the first group to mate with the second group. And when two groups can no longer successfully reproduce with each other, you have the birth of two new distinct species. Gagneux and his fellow researchers were able to demonstrate this effect by artificially exposing chimp sperm, which has Neu5Gc, to human antibodies. The antibodies consistently eliminated the chimp sperm before conception could ever have taken place.


Subsequent experiments with genetically altered mice - some of whom carried Neu5GC while the rest carried Neu5Gc-resistant antibodies - suggests the fertility rate between the two groups didn't drop immediately to zero, but rather it slowly became more and more difficult for successful reproduction to occur. Gagneux explains that this slow process actually makes speciation easier than a sudden drop, perhaps because it allows for the divergent populations to stabilize before being completely isolated from one another.

In any event, this is evidence for an evolutionary process known as speciation by infection, in which diseases can actually make one population reproductively incompatible with another. We know from previous studies that our ancestors lost Neu5Gc right around the same time as when Homo erectus first emerged, lending credence to the idea that, rather remarkably, infection and sugar helped put us on our current evolutionary path.

Via PNAS. Image of Homo erectus by Smithsonian National Museum of Natural History's Human Origins Program. Graphic by UC San Diego School of Medicine.